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Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study
BACKGROUND: Corneal neovascularization (CNV) is an important disease that causes blindness. Secretogranin III (Scg3) has emerged as a new influencing factor of neovascularization. This study analyzed the Scg3 antibody’s inhibitory effect on CNV and and explored its preliminary mechanism. METHODS: Hu...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9703748/ https://www.ncbi.nlm.nih.gov/pubmed/36443679 http://dx.doi.org/10.1186/s12886-022-02690-7 |
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author | Jin, He Yang, Binbin Jiang, Dongdong Ding, Zhixiang Xiong, Yu Zeng, Xinsheng |
author_facet | Jin, He Yang, Binbin Jiang, Dongdong Ding, Zhixiang Xiong, Yu Zeng, Xinsheng |
author_sort | Jin, He |
collection | PubMed |
description | BACKGROUND: Corneal neovascularization (CNV) is an important disease that causes blindness. Secretogranin III (Scg3) has emerged as a new influencing factor of neovascularization. This study analyzed the Scg3 antibody’s inhibitory effect on CNV and and explored its preliminary mechanism. METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with Scg3 and anti-Scg3. Cell proliferation, wound healing migration and tube formation assays were performed. Healthy adult New Zealand rabbits were randomly selected to be alkali burned and establish the corneal neovascularization (CNV) model. The rabbits were randomly divided into 3 groups (the high concentration group, low concentration group and control group). Different doses of anti-Scg3 and PBS were administered to the rabbits. Clinical examinations, immunostaining, quantitative real-time polymerase chain reaction (qPCR) and western blotting analyses were performed postoperatively. RESULTS: In the in vitro study, the Scg3 antibody mixture inhibited Scg3-induced endothelial cell proliferation and angiogenesis. In the in vivo study, significant CNV was observed in the control group. Confocal microscopy also revealed considerable active neovascularization in the control group. There was no obvious CNV growth in the high concentration group. Additionally, CD31, LYVE1 and CD45 expression was significantly inhibited after treatment with a high concentration of Scg3 antibody. The qPCR and western blotting analyses revealed that the levels of ERK in the low concentration group and high concentration group were higher than those in the control group at 7 days and 14 days. The levels of VEGF in the control group were significantly increased compared with those in the high concentration group. In all three groups, the levels of Akt were not significantly different at any time point. CONCLUSION: The expression of Scg3 could affect the growth of HUVECs in vitro. Treatment with a high concentration (0.5 µg/mL) of Scg3 antibody reduced the inflammatory response and inhibited the growth of corneal neovascularization after corneal alkali burn injury in rabbits. The MEK/ERK pathway might play an important role in the inhibitory effect of anti-Scg3. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12886-022-02690-7. |
format | Online Article Text |
id | pubmed-9703748 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-97037482022-11-29 Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study Jin, He Yang, Binbin Jiang, Dongdong Ding, Zhixiang Xiong, Yu Zeng, Xinsheng BMC Ophthalmol Research BACKGROUND: Corneal neovascularization (CNV) is an important disease that causes blindness. Secretogranin III (Scg3) has emerged as a new influencing factor of neovascularization. This study analyzed the Scg3 antibody’s inhibitory effect on CNV and and explored its preliminary mechanism. METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with Scg3 and anti-Scg3. Cell proliferation, wound healing migration and tube formation assays were performed. Healthy adult New Zealand rabbits were randomly selected to be alkali burned and establish the corneal neovascularization (CNV) model. The rabbits were randomly divided into 3 groups (the high concentration group, low concentration group and control group). Different doses of anti-Scg3 and PBS were administered to the rabbits. Clinical examinations, immunostaining, quantitative real-time polymerase chain reaction (qPCR) and western blotting analyses were performed postoperatively. RESULTS: In the in vitro study, the Scg3 antibody mixture inhibited Scg3-induced endothelial cell proliferation and angiogenesis. In the in vivo study, significant CNV was observed in the control group. Confocal microscopy also revealed considerable active neovascularization in the control group. There was no obvious CNV growth in the high concentration group. Additionally, CD31, LYVE1 and CD45 expression was significantly inhibited after treatment with a high concentration of Scg3 antibody. The qPCR and western blotting analyses revealed that the levels of ERK in the low concentration group and high concentration group were higher than those in the control group at 7 days and 14 days. The levels of VEGF in the control group were significantly increased compared with those in the high concentration group. In all three groups, the levels of Akt were not significantly different at any time point. CONCLUSION: The expression of Scg3 could affect the growth of HUVECs in vitro. Treatment with a high concentration (0.5 µg/mL) of Scg3 antibody reduced the inflammatory response and inhibited the growth of corneal neovascularization after corneal alkali burn injury in rabbits. The MEK/ERK pathway might play an important role in the inhibitory effect of anti-Scg3. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12886-022-02690-7. BioMed Central 2022-11-28 /pmc/articles/PMC9703748/ /pubmed/36443679 http://dx.doi.org/10.1186/s12886-022-02690-7 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Jin, He Yang, Binbin Jiang, Dongdong Ding, Zhixiang Xiong, Yu Zeng, Xinsheng Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study |
title | Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study |
title_full | Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study |
title_fullStr | Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study |
title_full_unstemmed | Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study |
title_short | Inhibitory effect of anti-Scg3 on corneal neovascularization: a preliminary study |
title_sort | inhibitory effect of anti-scg3 on corneal neovascularization: a preliminary study |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9703748/ https://www.ncbi.nlm.nih.gov/pubmed/36443679 http://dx.doi.org/10.1186/s12886-022-02690-7 |
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